Inflammatory markers and endometriosis

What can I say? It's complicated.

Endometriosis is an inflammatory disease, so a lot of people have questions about blood tests that look at inflammation. Let's look at what inflammatory markers are and specifically at CRP:

"Serum proteins that are produced in response to inflammation can be referred to as inflammatory markers. These proteins are mainly produced by the liver in response to stress and can also be called acute phase reactants. Pro-inflammatory cytokines such as IL-1, IL-6, and TNF-alpha induce synthesis of some acute phase reactants that include CRP, fibrinogen and haptoglobin. Other proteins, like albumin, are not sensitive to inflammatory cytokines for increased synthesis; instead chronic stress (inflammation) results in a lower synthesis rate with resultant decreased serum concentrations. The inflammatory markers are not diagnostic of inflammation, but reflect abnormalities that are seen in autoimmune diseases, infections, malignancies and other illnesses.

C-reactive protein (CRP)

"C-reactive protein (CRP/CRP-high sensitivity) was discovered and named for its reactivity to the C polysaccharide in the cell wall of S. pneumoniae. CRP, an innate immune protein, helps opsonize pathogens for phagocytosis and activates the complement system. CRP production is under the control of IL-1, IL-6, and TNF-alpha. Changes in serum CRP concentration change more quickly than ESR and therefore CRP may be a better reflection of current inflammation. Unlike the ESR, CRP is a fairly stable serum protein whose measurement is not time-sensitive and is not affected by other serum components. The magnitude of inflammation directly relates to the concentration of CRP. Levels < 0.2 mg/dl are considered normal, while those >1.0 mg/dL are suggestive off inflammation and/or infection. More recently, the use of high sensitivity CRP has been utilized. This test may better quantify lower levels of inflammation and has been important in evaluating cardiac disease and other inflammatory states.^{2, 3" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2832720/?report=reader}      

 

So what does this have to do with endometriosis?

Endometriosis is an inflammatory disease, so one might expect the markers to be high. But not necessarily in blood tests:

 

"Findings:

There was no significant difference between the CRP serum level in patients with endometriosis and infertile women without endometriosis. There was a significant difference in peritoneal level of CRP between case and control groups (p < 0.05).

Conclusions:

The findings suggested that measurement of this marker in patients’ serum or plasma cannot be used to diagnose endometriosis. It is further recommended that a combination of different markers might be helpful in this regard that could be studied in future."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3696960/

 

So we may not see an increase in the blood test but there is a difference in the peritoneal samples:

 

"Compared to the control group, the CRP level of the peritoneal fluid were higher in patients with endometriosis (p<0.05). Pelvic endometriosis is a chronic inflammatory disease that is in association with a general inflammatory response in the peritoneal cavity.[34,35] This disease is known to have an immunological background.[36] Macrophage constitutes 82- 99% of the all the cell population of peritoneal fluid.[37–39] Literature has repeatedly reported an increase of total peritoneal fluid cell numbers, cell concentration and macrophages in endometriosis patients in compare to the control.[40–43] The study of Dunselman et al. also confirmed that there is an increase in the number and concentration of peritoneal cells in patients with endometriosis as compared to the control group.[38]" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3696960/

 

While we're on the subject, let's discuss CA-125 levels:

 

It's a test that looks at markers for certain cancers, but if your doctor orders it and it's high, don't let it scare you. "...many noncancerous conditions can increase the CA 125 level.

Many different conditions can cause an increase in CA 125, including normal conditions, such as menstruation, and noncancerous conditions, such as uterine fibroids." http://www.mayoclinic.org/tests-procedures/ca-125-test/basics/definition/prc-20009524 It can also be high in people with endometriosis: "Studies published since continue to demonstrate a correlation between raised CA125 levels and endometriosis (Abrao et al., 1999; Somigliana et al., 2004; Agic et al., 2008; Seeber et al., 2008), and some imply a correlation with stage of disease (Chen et al., 1998; Amaral et al., 2006; Martinez et al., 2007; Rosa e Silva et al., 2007). One study has indicated that CA125 may be more accurate at diagnosing women with later stages of disease, in concordance with the review by Mol (Maiorana et al., 2007)." http://humupd.oxfordjournals.org/content/16/6/651.full 

Remember, all these tests might be a mere indication of endometriosis, but they are very nonspecific. The only way to accurately diagnose endometriosis is through surgery.

Mast cells:

"Mast cells may contribute to the development of pain and hyperalgesia in endometriosis
October 2006
The presence of increased activated and degranulating mast cells in deeply infiltrating endometriosis, which are the most painful lesions, and the close histological relationship between mast cells and nerves strongly suggest that mast cells could contribute to the development of pain and hyperalgesia in endometriosis, possibly by a direct effect on nerve structures.

Researchers set out to detect and quantify mast cells in peritoneal, ovarian, and deep infiltrating endometriosis and to study the relationship between mast cells and nerves in endometriosis.

Excision of endometriosis from different anatomical locations was undertaken in 69 women, who were undergoing laparoscopic excision of endometriosis for pain. Thirty-seven biopsies of normal tissue were obtained from women without endometriosis.
The women with deeply infiltrating lesions had significantly higher preoperative pain scores than women with peritoneal or ovarian endometriosis. Mast cells and degranulating mast cells are significantly more abundant in endometriotic lesions than in non-affected tissues. Deep infiltrating lesions show a significantly higher number of mast cells, activated mast cells, and mast cells located <25 mum from nerves than peritoneal and ovarian lesions. The authors found significantly more degranulating mast cells in deep infiltrating lesions than in peritoneal lesions.
Source

Anaf V, Chapron C, El Nakadi I, De Moor V, Simonart T, Noel JC. Pain, mast cells, and nerves in peritoneal, ovarian, and deep infiltrating endometriosis. Fertil Steril 2006;86(5):1336-43"

http://endometriosis.org/news/research/mast-cells-contribute-to-development-of-pain-and-hyperalgesia-in-endometriosis/

 

For a lot more on peripheral biomarkers of endometriosis see: http://humupd.oxfordjournals.org/content/16/6/651.full

  "Endometriotic lesion removal significantly alters the inflammatory profile both locally and systemically in women with endometriosis. Our findings indicate that ectopic lesions are the major drivers of systemic inflammation in endometriosis." http://www.ncbi.nlm.nih.gov/pubmed/26698677 

A few things that have helped me

Everyone is different with what will help them feel better. For me, a healthy diet with some specific changes and yoga are what I have found help me the most.

 

Specific diet changes include going gluten free (there has been research to support  this in endo patients- http://endocomprehensive.blogspot.com/2014/03/gluten-free-and-endo.html), eating food as close to nature as possible/least processed, avoiding my trigger foods (lactose, gluten, cruciferous veggies, etc- see the FODMAPs diet for IBS), and reducing sugary foods/bad carbs.

 

I also found the following items the most helpful to include in my diet:

 

Plenty of clear fresh water. Add in some lemon. Spring water seems to help the most, but I have a water filter too.

 Blueberries (probably any berry would be good)

 

Spinach. I don't whether it's the iron, the magnesium, or what, but organic spinach helps.

 

Albacore tuna. I've gotten some great deals on sustainably caught, low mercury canned tuna. Perhaps the omega-3's that help?

 

 

 

Egg white protein powder. I make a smoothie with this and spinach and I can tell I feel better. I have wondered if the l glutamine helps my gut. I can tell a difference between the egg white versus the whey.

 

I think the extra B vitamins and perhaps the low dose of vitex in this drink mix help. I drink it in the morning in my green tea.

 

Again, eating organic whenever possible, seems to help.

 

 

Again, these are things that have helped me and are not recommendations for what will work with anyone else. I can't say it made my endometriosis better, but it did help my health overall and improve my ability to deal with my endo and its ramifications.

 

 

PS Here's a link to some of the yoga poses I find most helpful to me: http://endocomprehensive.blogspot.com/2014/07/my-current-yoga-poses-that-help.html 

 

Similar stem cells, different gene exclusions

"Tissue of DIE and SE appears to have similar stem cell-related genes. Nevertheless, there are differences in gene expression between SE and DIE." So the stem cells of superficial and deep infiltrating endometriosis are similar but the gene expression is different. So what causes the deep infiltrating to be expressed differently? Hormonal influence? Diet? Toxins? http://www.ncbi.nlm.nih.gov/pubmed/26426155

Since endo is most likely laid down embryonically, I don't know that this necessarily points to pathogenesis of endo (especially as the levels decrease after the removal of the lesions) but the presence of endo certainly produces an inflammatory state.

 

J Immunol. 2015 Aug 10. pii: 1501138.

IL-17A Contributes to the Pathogenesis of Endometriosis by Triggering Proinflammatory Cytokines and Angiogenic Growth Factors.

Ahn SH¹, Edwards AK¹, Singh SS², Young SL³, Lessey BA⁴, Tayade C⁵.

Author information

• ¹Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario K7L 3N6, Canada;
• ²Department of Obstetrics and Gynecology, University of Ottawa, Ottawa, Ontario K1H 7W9, Canada;
• ³Department of Obstetrics and Gynecology, University of North Carolina, Chapel Hill, NC 27514; and.
• ⁴Department of Obstetrics and Gynecology, Greenville Health System, Greenville, SC 29605.
• ⁵Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario K7L 3N6, Canada; tayadec@queensu.ca.

Abstract

Endometriosis is a chronic, inflammatory disease characterized by the growth of endometrial tissue in aberrant locations outside the uterus. Neoangiogenesis or establishment of new blood supply is one of the fundamental requirements of endometriotic lesion survival in the peritoneal cavity. IL-17A is emerging as a potent angiogenic and proinflammatory cytokine involved in the pathophysiology of several chronic inflammatory diseases such as rheumatoid arthritis and psoriasis. However, sparse information is available in the context of endometriosis. In this study, we demonstrate the potential importance of IL-17A in the pathogenesis and pathophysiology of endometriosis. The data show a differential expression of IL-17A in human ectopic endometriotic lesions and matched eutopic endometrium from women with endometriosis. Importantly, surgical removal of lesions resulted in significantly reduced plasma IL-17A concentrations. Immunohistochemistry revealed localization of IL-17A primarily in the stroma of matched ectopic and eutopic tissue samples. In vitro stimulation of endometrial epithelial carcinoma cells, Ishikawa cells, and HUVECs with IL-17A revealed significant increase in angiogenic (vascular endothelial growth factor and IL-8), proinflammatory (IL-6 and IL-1β), and chemotactic cytokines (G-CSF, CXCL12, CXCL1, and CX3CL1). Furthermore, IL-17A promoted tubulogenesis of HUVECs plated on Matrigel in a dose-dependent manner. Thus, we provide the first evidence, to our knowledge, that endometriotic lesions produce IL-17A and that the removal of the lesion via laparoscopic surgery leads to the significant reduction in the systemic levels of IL-17A. Taken together, our data show a likely important role of IL-17A in promoting angiogenesis and proinflammatory environment in the peritoneal cavity for the establishment and maintenance of endometriosis lesions.
Copyright © 2015 by The American Association of Immunologists, Inc.

Origins of endo

From Endometriosis Update blog (lots of good info- check it out!!):

"Several studies have focused on characterising the endometrium of women with and without endometriosis and found that; yes the endometrium in women with endometriosis is indeed different. The endometrium from women with endometriosis appears to have a higher ability to survive, proliferate and invade, seemingly filling in the missing part of the retrograde menstruation theory.

But, like all great mystery stories, the case is never wrapped up in a neat little package so early on. In recent years more and more evidence is coming to the fore, challenging the theory of retrograde menstruation. In particular there is now quite a significant amount of evidence to show the displaced endometrium that defines endometriosis is, in fact, present before you were even born. There are also rare documented cases of endometriosis in men, women who cannot menstruate and non-menstruating primates; so clearly there is the need for some radical re-thinking.

Maybe we’ve had the whole thing upside-down; maybe it is not the endometrium that dictates the fate of endometriosis, but endometriosis that dictates the fate of the endometrium. A collaborative research effort has provided some evidence to this very end (you can read the full article here). The authors of this study experimentally induced endometriosis in baboons by injecting endometrial cells into the pelvic cavity and letting them form endometriotic implants. They then compared the expression of genes within the endometrium of the baboons with experimentally induced endometriosis and disease free baboons over the course of 16 months. What they found was that the presence of endometriosis (even in its very early stages) led to marked changes (a total of 4,331 genes were altered) in the normal endometrium.

This potentially turns accepted wisdom on its head, in that women with endometriosis are not born with a defective endometrium that gives rise to endometriosis via retrograde menstruation. Rather, if we are to take all the above evidence into account, it appears endometriosis is a condition you are born with that, when the endometriotic implants ‘mature’ lead to changes in the function of the normal endometrium, thus perhaps also accounting for the fertility issues women with endo suffer from." http://www.endo-update.blogspot.co.uk/.../turning-on-its...

Peritoneal endo lesions nerve fibers

"RESULT(S): Pain-conducting substance-P-positive nerve fibers were found to be directly colocalized with human peritoneal endometriotic lesions in 74.5% of all cases. The endometriosis-associated nerve fibers are accompanied by immature blood vessels within the stroma. Nerve growth factor and neutrophin-3 are expressed by endometriotic cells. Growth-associated protein 43, a marker of neural outgrowth and regeneration, is expressed in endometriosis-associated nerve fibers but not in existing peritoneal nerves. CONCLUSION(S): The data provide the first evidence of direct contact between sensory nerve fibers and peritoneal endometriotic lesions. This implies that the fibers play an important role in the etiology of endometriosis-associated pelvic pain. Moreover, emerging evidence suggests that peritoneal endometriotic cells exhibit neurotrophic properties." http://www.ncbi.nlm.nih.gov/pubmed/17412328

 

"RESULT(S): Peritoneal endometriosis-associated nerve fibers were found significantly more frequently in group A than in group B (82.6% vs. 33.3%). CONCLUSION(S): The present study suggests that the presence of endometriosis-associated nerve fibers in the peritoneum is important for the development of endometriosis-associated pelvic pain and dysmenorrhea." http://www.ncbi.nlm.nih.gov/pubmed/18980761

 

"RESULT(S): Lesions from the rectovaginal septum were significantly more likely to be associated with a nerve fiber and report more menstrual pain than lesions from other regions. The PF glycodelin concentrations were also significantly higher in samples with an endometriotic-associated nerve. In peritoneal endometriotic lesions significantly more menstrual pain was reported when endometriotic lesions were associated with nerve fibers, although no difference was observed between the cytokine concentrations. Ovarian endometriotic lesions were rarely associated with nerve fibers.
CONCLUSION(S):
The presence of endometriosis-associated nerve fibers appear to be related to both the pain experienced by women with endometriosis and the concentration of PF cytokines; however, this association varies with the lesion location." http://www.ncbi.nlm.nih.gov/pubmed/22154765


"There was no difference in the density of nerve fibers across the menstrual cycle in peritoneal endometriotic lesions. These findings may explain why patients with peritoneal endometriosis often have painful symptoms throughout the menstrual cycle." http://www.ncbi.nlm.nih.gov/pubmed/21334610


"Progestogens and combined oral contraceptives reduced nerve fiber density and nerve growth factor and nerve growth factor receptor p75 expression in peritoneal endometriotic lesions." http://www.ncbi.nlm.nih.gov/pubmed/18976764

"Pain generation in EM is an intricate interplay of several factors such as the endometriotic lesions themselves and the pain-mediating substances, nerve fibres and cytokine-releasing immune cells such as macrophages. These interactions seem to induce a neurogenic inflammatory process. Recently published data demonstrated an increased peptidergic and decreased noradrenergic nerve fibre density in peritoneal lesions. These data could be substantiated by in vitro analyses demonstrating that the peritoneal fluids of patients suffering from EM induced an enhanced sprouting of sensory neurites from chicken dorsal root ganglia and decreased neurite outgrowth from sympathetic ganglia. These findings might be directly involved in the perpetuation of inflammation and pain. Furthermore, the evidence of EM-associated smooth muscle-like cells seems another important factor in pain generation. The peritoneal endometriotic lesion leads to reactions in the surrounding tissue and, therefore, is larger than generally believed. The identification of EM-associated nerve fibres and smooth muscle-like cells fuel discussions on the mechanisms of pain generation in EM, and may present new targets for innovative treatments." http://www.ncbi.nlm.nih.gov/pubmed/24590000

"We could detect an increased sensory and decreased sympathetic nerve fibres density in peritoneal lesions compared to healthy peritoneum. Peritoneal fluids of patients with endometriosis compared to patients without endometriosis induced an increased sprouting of sensory neurites from DRG and decreased neurite outgrowth from sympathetic ganglia. In conclusion, this study demonstrates an imbalance between sympathetic and sensory nerve fibres in peritoneal endometriosis, as well as an altered modulation of peritoneal fluids from patients with endometriosis on sympathetic and sensory innervation which might directly be involved in the maintenance of inflammation and pain." http://www.ncbi.nlm.nih.gov/pubmed/21888965

   

March is Endometriosis Awareness month!

 

March is endometriosis awareness month and yellow is the color! Here are a few pictures that I have run across that are useful for profile pictures, cover photos, and general awareness:

 

? Link Between PCOS and endometriosis

Old (from 1989): "Pelvic endometriosis was observed in 15 of 91 women (16.5%) with laparoscopically confirmed polycystic ovary syndrome. There were no significant clinical differences among those with and those without endometriosis. The groups were of similar age, parity, and ponderal indices and had similar incidences of oligomenorrhea, hirsutism, and infertility; the serum concentrations of LH, FSH, LH/FSH, prolactin, testosterone, and dehydroepiandrosterone sulfate were also similar in each group. However, women with polycystic ovaries and endometriosis presented more frequently with regular menses (40 versus 14.5%; P = .05) and less frequently with secondary amenorrhea (0 versus 38.2%; P = .05) and galactorrhea (0 versus 9.2%; P = .05) than the women with polycystic ovaries alone. Endometriosis appears to be a coincidental finding in polycystic ovary syndrome, and its development does not modify significantly the clinical picture or biochemical profiles of these patients. However, menstrual patterns seem to be affected." http://www.ncbi.nlm.nih.gov/pubmed/2797642

2011: "The endocrinologic and metabolic abnormalities of women with polycystic ovary syndrome (PCOS) can result in a series of endometrial diseases. Abnormalities of hyperandrogenism and hyperinsulinemia that may be found in PCOS can elevate the levels of E2 indirectly, reduce progesterone secretion and induce some growth factors such as vascular endothelial growth factor (VEGF) and insulin-like growth factors (IGFs) over expression, which may have a major impact on endometriosis occurrence and development. We suppose that there is a possible connection between PCOS and endometriosis." http://www.sciencedirect.com/.../pii/S1001784412600133

Surgical Technique and "microscopic" endo

"Occult or microscopic lesions have been reported as early as 1986 from laparotomy procedures. Hopton and Redwine {7} have shown a linear inverse relationship between the distance of the viewing lens from the peritoneal surface and the incidence of OME; these authors claim that OME almost ceases to exist with close contact laparoscopy with less than 1cm separation of the laparoscope tip from the peritoneal surface (and with direct visualisation laparoscopy, suggesting that the use of video-assisted laparoscopy may impair visualisation) with incidences of OME ranging from 0% to 25% in various studies {1-7}. 

 

"Hopton and Redwine {7} have also highlighted the key factors that are likely to be influential on whether OME is diagnosed: the definition of normal peritoneum, the size and location of biopsies of 'normal peritoneum', the histological definition of endometriosis, and whether women undergoing laparoscopic assessment have recently been using hormonal suppressive therapy....

 

"The more careful the search for endometriosis – and the closer the laparoscope tip is applied to the peritoneal surface – the less chance of missing any endometriosis. - There is a strong place for clear definitions to standardise laparoscopy performed by all gynaecological surgeons in relation to (a) viewing distance from the laparoscope tip and (b) definitions of what constitutes abnormal peritoneum, particularly the subtle abnormalities highlighted by Redwine {5} and Redwine and Yocom {6}. The more meticulous the search for endometriosis and the combination of this search with meticulous excision of all lesions, the more likely endometriosis is to be eradicated through laparoscopic surgery."

http://f1000.com/prime/718213409

Epigenetics in endo

Here is an interesting article discussing epigenetics in endometriosis. While they do assimilate epigenetics with pathogenesis of endo (since endo has been seen in fetuses, it is still more plausible that it is laid down embryonically), the incidence of epigenetics playing a role in how the disease presents itself and is influenced is interesting to consider.

 

 

http://molehr.oxfordjournals.org/content/15/10/587.long

 

 

Here's a tidbit:

 

"Endometriosis has been regarded as an ultimate hormonal disease, owing much to its estrogen-dependency and aberrations in estrogen production and metabolism (Bulun et al., 2002; Kitawaki et al., 2002; Gurates and Bulun, 2003). It also has been viewed as an immunological disease due to a myriad immunological aberration in endometriosis (Paul Dmowski and Braun, 2004; Ulukus and Arici, 2005). In addition, it has been thought of a disease caused by exposure to environmental pollution and toxins (Rier et al., 1993; Rier, 2002) although so far there are no solid human data (Guo, 2004). Finally, it has been regarded as a genetic disease (Simpson et al., 2003; Barlow and Kennedy, 2005), due, apparently, to its reported familial aggregation. Yet even the reported familial aggregation, when examined closely, may be debatable (Di and Guo, 2007), and there has been little progress regarding the identification of genetic variants that predispose women to endometriosis (Di and Guo, 2007; Falconer et al., 2007; Guo, 2009b)."

 

((((((NOTE: some of the references are dated- such as little progress to genetic variances when there have been such since then (2007).)))))

 

"Given the reported epigenetic aberrations in endometriosis, one question is whether these aberrations are the cause or merely the consequence of endometriosis. Since most, if not all, human studies reporting epigenetic aberrations in endometriosis are carried out cross-sectionally, the reported aberration may be a cause for, but also could be a consequence of, endometriosis.

 

"Aging (Wilson and Jones, 1983; Toyota and Issa, 1999; Richardson, 2002), diet (Jacob et al., 1998), chronic inflammation (Hsieh et al., 1998; Issa et al., 2001), prolonged transcriptional suppression (Song et al., 2002; Stirzaker et al., 2004) and even maternal care (Champagne et al., 2006). In endometriosis, it has been shown that prolonged stimulation of an endometriotic epithelial-like cell line by tumor necrosing factor (TNFα), which has been shown to have increased production in endometriosis, resulted in at least partial methylation in the PR-B promoter (Wu et al., 2008b). This provides evidence that certain phenotypic changes in endometriosis, such as increased production of proinflammatory cytokines, may also cause epigenetic aberrations, which in turn result in changes in gene expression and subsequently other phenotypic changes such as increased cellular proliferation (Wu et al., 2008a) and perhaps some phenotypic changes."

 

http://molehr.oxfordjournals.org/content/15/10/587.long

 

genotypes of GSTM1 and/or GSTT1 contribute to risk of endometriosis

"Endometriosis is one of the most frequent benign gynecological disorders. Numerous studies have shown an association between GSTM1 and/or GSTT1 polymorphisms and endometriosis susceptibility. However, these associations remain inconclusive. To derive a more precise estimation, we conducted a comprehensive search to identify all existing studies and then performed a meta-analysis. Electronic literature searches of the PubMed, Chinese Biomedical, and China National Knowledge Infrastructure databases were performed up to December 2013. GSTM1-, GSTT1-, and dual-null genotypes were analyzed independently, and pooled odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated by comparing the null genotype with other genotypes using the random-effects or fixed-effects model. Twenty-five and 16 independent studies on GSTM1 and GSTT1 polymorphisms, respectively, and five GSTM1-GSTT1 interaction analyses were identified and included in this meta-analysis. Both GSTM1- and GSTT1-null genotypes increased risk of endometriosis (OR = 1.54, 95% CI: 1.30–1.83, P<0.001; OR = 1.41, 95% CI: 1.10–1.82, P = 0.007; respectively). Moreover, we found a significant positive association between the dual null genotype GSTM1-GSTT1 and endometriosis susceptibility (OR = 1.33, 95% CI: 1.03–1.72, P = 0.027). This meta-analysis provides evidence that null genotypes of GSTM1 and/or GSTT1 contribute to risk of endometriosis. Further investigations are required to confirm these findings." http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0106761

Links endo after ovary removal

http://www.ncbi.nlm.nih.gov/pubmed/8127534

http://www.ncbi.nlm.nih.gov/pubmed/7589631

http://link.springer.com/chapter/10.1007/978-1-4613-8404-5_18#page-1

http://www.ncbi.nlm.nih.gov/pubmed/11789754

http://onlinelibrary.wiley.com/doi/10.1111/j.1471-0528.1999.tb08377.x/full

http://www.researchgate.net/publication/12870281_Recurrent_pain_after_hysterectomy_and_bilateral_salpingo-oophorectomy_for_endometriosis_evaluation_of_laparoscopic_excision_of_residual_endometriosis

http://endometriosis.org/treatments/hysterectomy/

Exercise and Endometriosis

Pain with exercise can be a symptom of endometriosis. The inflammation, the location of the lesions, the presence of adhesions, and other factors such as pelvic floor dysfunction (too tight muscles- http://endocomprehensive.blogspot.com/2014/01/pelvic-floor-spasm.html), trigger points, muscles spasms, etc can all factor into the pain felt. So how is exercise good for endometriosis?

 

"Regular physical exercise seems to have protective effects against diseases that involve inflammatory processes since it induces an increase in the systemic levels of cytokines with anti-inflammatory and antioxidant properties and also acts by reducing estrogen levels. Evidence has suggested that the symptoms associated with endometriosis result from a local inflammatory peritoneal reaction caused by ectopic endometrial implants....regular physical exercise seems to have protective effects against diseases that involve inflammatory processes since it induces an increase in the systemic levels of cytokines with anti-inflammatory properties [9]. In addition, regular physical exercise is associated with a cumulative effect of reduction of menstrual flow, of ovarian stimulation and of the action of estrogen [10]....Analysis of available literature data show that there are no controlled and randomized studies identifying whether physical exercise prevents the occurrence or progression of the endometriosis and how and to what extent physical exercise could be beneficial for women with endometriosis. The few existing studies are of an observational type, with little or no statistical significance, but that indicate an inverse relationship between the practice of physical exercise and the risk of endometriosis. These studies also drawing attention to the possibility that conclusions about non-protective effect of exercise in women with endometriosis can be due the discomfort experienced, what prevent the practice of physical exercise. Therefore, with the literature available it is not possible to point out the real role of physical exercise in endometriosis. Thus, until now we only have speculations about this topic. In this respect, we believe that studies well controlled, using validated instruments for evaluation and follow up, well- defined study groups and well established exercise protocol can demonstrate the real role of physical exercise on treatment of endometriosis. On this basis, experimental models of endometriosis would be justified because they would permit the characterization of the time course of the disease in order to elucidate whether physical exercise is indeed able to interfere with the development of the endometriosis injury. In addition, it would be possible to determine what intensity would be necessary for physical exercise to be used in both a preventive and curative manner regarding the disease." http://www.rbej.com/content/12/1/4

 

Exercise can be helpful for most chronic pain conditions:

 

 

"“Exercise improves your pain threshold,” says Trent Nessler, PT, DPT, MPT, a vice president with Champion Sports Medicine in Birmingham, Ala. “With chronic pain, your pain threshold drops -- in other words, it takes less pain to make you feel more uncomfortable. With cardiovascular, strengthening, and flexibility exercise, you can improve that pain threshold.”" http://www.webmd.com/pain-management/features/exercise-relief

 

"Dr Sluka concluded that these data suggest that regular exercise reduces pain by activation of opioid receptors in descending inhibitory pathways in the central nervous system. She further proposed that regular exercise could prevent the transition from acute to chronic pain through the release of regulatory macrophages and increased levels of IL-10, an anti-inflammatory cytokine which can reduce nociceptor sensitisation [2]." http://www.bodyinmind.org/physical-activity-chronic-pain/

 

"Exercise helps to alleviate pain related to nerve damage (neuropathic pain) by reducing levels of certain inflammation-promoting factors, suggests an experimental study in the June issue of Anesthesia & Analgesia, official journal of the International Anesthesia Research Society (IARS)." http://www.eurekalert.org/pub.../2012-06/wkh-hde060112.php

 

 

But any exercise regimen should be tailored for your body and is best done under the guidance of a professional who is familiar with your condition.

"Exercise activates endogenous analgesia in healthy individuals. The increased pain threshold following exercise is due to the release of endogenous opioids and activation of (supra)spinal nociceptive inhibitory mechanisms orchestrated by the brain. Exercise triggers the release of beta-endorphins from the pituitary (peripherally) and the hypothalamus (centrally), which in turn enables analgesic effects by activating μ-opioid receptors peripherally and centrally, respectively. The hypothalamus, through its projections on the periaqueductal grey, has the capacity to activate descending nociceptive inhibitory mechanisms. However, several groups have shown dysfunctioning of endogenous analgesia in response to exercise in patients with chronic pain. Muscle contractions activate generalized endogenous analgesia in healthy, pain-free humans and patients with either osteoarthritis or rheumatoid arthritis, but result in increased generalised pain sensitivity in fibromyalgia patients. In patients having local muscular pain (e.g. shoulder myalgia), exercising non-painful muscles activates generalized endogenous analgesia. However, exercising painful muscles does not change pain sensitivity either in the exercising muscle or at distant locations. LIMITATIONS: The reviewed studies examined acute effects of exercise rather than long-term effects of exercise therapy. CONCLUSIONS: A dysfunctional response of patients with chronic pain and aberrations in central pain modulation to exercise has been shown, indicating that exercise therapy should be individually tailored with emphasis on prevention of symptom flares. The paper discusses the translation of these findings to rehabilitation practice together with future research avenues." http://www.ncbi.nlm.nih.gov/pubmed/22786458

 

Pelvic physical therapy helped me get started by helping to retrain my pelvic muscles to relax and knowing what would trigger more pain (high impact exercises). (For some of the things pelvic PT can help with see http://www.pelvicpainrehab.com/female-pelvic-pain/674/how-pelvic-floor-pt-helps-endometriosis-4/ or watch this video: http://endocomprehensive.blogspot.com/2013/11/video-endometriosis-and-pelvic-physcial.html) After I had excision surgery, we were able to move on to rebalancing my muscle groups with a balance of strengthening and stretching exercises.

 

My mainstay throughout has been yoga. Many of the exercises I did in pelvic PT were what  I was doing in yoga. Yoga not only helped me manage pain but also manage the stress caused by the pain. For some of the poses that have helped me, see http://endocomprehensive.blogspot.com/2014/07/my-current-yoga-poses-that-help.html. Also here is a video that I come back to often: http://www.yogajournal.com/video/video/gentle-flow/